Abstract : A standardized compression injury of rat spinal cord brought about a time‐dependent biphasic production of thromboxane A2 (detected as thromboxane B2) and prostaglandin I2 (detected as 6‐ketoprostaglandin F1α. Thromboxane B2 was predominant during the first 1 h, whereas the 6‐ketoprostaglandin F1α level exceeded that of thromboxane B2 at 8 h postinjury. As examined by inhibitor experiments and northern blotting, cyclooxygenase‐1 was responsible for the first phase, and cyclooxygenase‐2 was involved in the second phase. On compression injury the levels of interleukin‐1α and ‐1β detected as mRNA and protein increased and peaked at 2‐4 h. Injection of exogenous interleukin‐1 α into the spinal cord resulted in an increase of cyclooxygenase‐2 mRNA content and a predominant production of 6‐ketoprostaglandin F1α resembling the second phase of eicosanoid production. Concomitantly, extravascular migration of polymorphonuclear leukocytes was enhanced after the interleukin‐1α injection. These cells together with vascular endothelial cells and glial cells were stained positively with an anti‐cyclooxygenase‐2 antibody. The results suggest that the immediate eicosanoid synthesis after spinal cord injury was due to the constitutive cyclooxygenase‐1 and the delayed synthesis of eicosanoids was attributable to the induction of cyclooxygenase‐2 mediated by interleukin‐1 α.
Journal of Neurochemistry – Wiley
Published: Jan 1, 1999
Keywords: ; ; ; ;
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